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Poole, Emma, Huang, Christopher J. Z., Forbester, Jessica, Shnayder, Miri, Nachshon, Aharon, Kweider, Baraa, Basaj, Anna, Smith, Daniel, Jackson, Sarah Elizabeth, Liu, Bin, Shih, Joy, Kiskin, Fedir N., Roche, K., Murphy, E., Wills, Mark R., Morrell, Nicholas W., Dougan, Gordon, Stern-Ginossar, Noam, Rana, Amer A. 
ORCID: https://orcid.org/0000-0002-2330-4643 and Sinclair, John
(2019)
An iPSC-derived myeloid lineage model of herpes virus latency and reactivation.
Frontiers in Microbiology, 10.
ISSN 1664-302X
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Abstract
Herpesviruses undergo life-long latent infection which can be life-threatening in the immunocompromised. Models of latency and reactivation of human cytomegalovirus (HCMV) include primary myeloid cells, cells known to be important for HCMV latent carriage and reactivation in vivo. However, primary cells are limited in availability, and difficult to culture and to genetically modify; all of which have hampered our ability to fully understand virus/host interactions of this persistent human pathogen. We have now used iPSCs to develop a model cell system to study HCMV latency and reactivation in different cell types after their differentiation down the myeloid lineage. Our results show that iPSCs can effectively mimic HCMV latency/reactivation in primary myeloid cells, allowing molecular interrogations of the viral latent/lytic switch. This model may also be suitable for analysis of other viruses, such as HIV and Zika, which also infect cells of the myeloid lineage.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | sdg 3 - good health and well-being ,/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_being |
| Faculty \ School: | Faculty of Science > School of Biological Sciences |
| Related URLs: | |
| Depositing User: | LivePure Connector |
| Date Deposited: | 11 Nov 2020 01:15 |
| Last Modified: | 22 Oct 2022 07:26 |
| URI: | https://ueaeprints.uea.ac.uk/id/eprint/77624 |
| DOI: | 10.3389/fmicb.2019.02233 |
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